Evidence map›Paper›PMID 28404891›Full record

ArticleOncotarget2017

HMGB1 promotes differentiation syndrome by inducing hyperinflammation via MEK/ERK signaling in acute promyelocytic leukemia cells.

Lanlan Tang, Wenwen Chai, Fanghua Ye, Yan Yu, Lizhi Cao, Minghua Yang, Min Xie, Liangchun Yang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 28 citations in OpenAlex.

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  16. Inhibiting ERK/Mnk/eIF4E broadly sensitizes ovarian cancer response to chemotherapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2018
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Lanlan TangDepartment of Pediatrics, Xiangya Hospital, Central South University, Changsha, Hunan 410008, People's Republic of China.
Wenwen ChaiDepartment of Nuclear Medicine, Hunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan 410008, People's Republic of China.
Fanghua YeDepartment of Pediatrics, Xiangya Hospital, Central South University, Changsha, Hunan 410008, People's Republic of China.
Yan YuDepartment of Pediatrics, Xiangya Hospital, Central South University, Changsha, Hunan 410008, People's Republic of China.
Lizhi CaoDepartment of Pediatrics, Xiangya Hospital, Central South University, Changsha, Hunan 410008, People's Republic of China.
Minghua YangDepartment of Pediatrics, Xiangya Hospital, Central South University, Changsha, Hunan 410008, People's Republic of China.
Min XieDepartment of Pediatrics, Xiangya Hospital, Central South University, Changsha, Hunan 410008, People's Republic of China.
Liangchun YangDepartment of Pediatrics, Xiangya Hospital, Central South University, Changsha, Hunan 410008, People's Republic of China.
Central South University · CNXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Differentiation therapy based on all-trans-retinoic acid (ATRA) and arsenic trioxide (ATO) for the treatment of acute promyelocytic leukemia (APL) is complicated by the development of differentiation syndrome (DS), which can be fatal. We examined the role of HMGB1 (high-mobility group box 1) in DS using both in vitro and in vivo models. HMGB1 and the pro-inflammatory cytokines IL-1β and TNF-α were gradually released from NB4 and HL-60 cells treated with ATRA and/or ATO. Similarly, higher serum HMGB1 levels positively correlated with the clinical status of DS patients. Exogenous HMGB1 promoted rapid release of IL-1β and TNF-α as well as elevated expression of ICAM-1, without altering cell differentiation. Exogenous HMGB1 also enhanced pulmonary infiltration and up-regulated ICAM-1 expression in the ATRA-treated DS mouse. Pharmacological inhibition or depletion of MEK1/2 reduced the cytokine levels and suppressed expression of ICAM-1 and the adhesion of HMGB1-treated NB4 cells to endothelial cells, implicating MEK/ERK signaling in the response to HMGB1 during DS. Treatment with a HMGB1-neutralizing antibody reduced secretion of TNF-α and IL-1β, arrested the elevation of ICAM-1 and blunted the activation of ERK1/2 in ATRA-induced NB4 cells. The HMGB1-neutralizing antibody also decreased ICAM-1 expression and reduced mortality in ATRA-treated DS model mice. These findings demonstrate that released HMGB1 is central to DS, and that targeting HMGB1 may be of therapeutic value in the treatment of DS.

Indexed as

Cell DifferentiationMAP Kinase Signaling SystemAdolescentAnimalsAntineoplastic Combined Chemotherapy ProtocolsCell Adhesion MoleculesCell Line, TumorCell SurvivalChildChild, PreschoolCytokinesDisease Models, AnimalFemaleGene Expression Regulation, NeoplasticHMGB1 ProteinHumansCell Adhesion MoleculesCytokinesHMGB1 ProteinInflammation Mediatorsadhesive moleculecytokinesdifferentiation syndromeHMGB1MEK/ERK

Identifiers

PMID28404891
PMCPMC5432337
OpenAlexW2588871338

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.